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Results Time-Course of Cell Growth and comet formation in DU 145 prostate cancer and TP 366 glioblastoma cells provoked by TMZ and TMZ-BioShuttle dilu-tion series Two different cell l

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International Journal of Medical Sciences

ISSN 1449-1907 www.medsci.org 2008 5(5):273-284

© Ivyspring International Publisher All rights reserved Research Paper

TMZ-BioShuttle – a reformulated Temozolomide

Waldemar Waldeck1, Manfred Wiessler2, Volker Ehemann3, Ruediger Pipkorn4, Herbert Spring5, Juergen Debus6, Bernd Didinger6, Gabriele Mueller1, Joerg Langowski1, Klaus Braun2

1 German Cancer Research Center, Division of Biophysics of Macromolecules, INF 580, D-69120 Heidelberg, Germany

2 German Cancer Research Center, Dept of Molecular Toxicology, INF 280, D-69120 Heidelberg, Germany

3 University of Heidelberg, Institute of Pathology, INF 220, D-69120 Heidelberg, Germany

4 German Cancer Research Center, Central Peptide Synthesis Unit, INF 580, D-69120 Heidelberg, Germany

5 German Cancer Research Center, Dept of Structural Analysis of Gene Structure and Function, INF 280, D-69120 Heidel-berg, Germany

6 University of Heidelberg, Dept of Radiation Oncology, INF 400, D-69120 Heidelberg, Germany

280, D-69120 Heidelberg, Germany Phone: +49 6221-42 2495; Fax: +49 6221-42 3375; e-mail: k.braun@dkfz.de

Received: 2008.08.18; Accepted: 2008.09.12; Published: 2008.09.15

There is a large number of effective cytotoxic drugs whose side effect profile, efficacy, and long-term use in man are well understood and documented over decades of use in clinical routine e.g in the treatment of recurrent glioblastoma multiforme (GBM) and the hormone-refractory prostate cancer (HRPC) Both cancers are insensitive against most chemotherapeutic interventions; they have low response rates and poor prognoses Some cytotoxic agents can be significantly improved by using modern technology of drug delivery or formulation We succeeded

to enhance the pharmacologic potency with simultaneous reduction of unwanted adverse reactions of the highly efficient chemotherapeutic temozolomide (TMZ) as an example The TMZ connection to transporter molecules (TMZ-BioShuttle) resulted in a much higher pharmacological effect in glioma cell lines while using reduced doses This permits the conclusion that a suitable chemistry could realize the ligation of pharmacologically active, but sensitive and highly unstable pharmaceutical ingredients without functional deprivation The re-formulation

of TMZ to TMZ-BioShuttle achieved a nearly 10-fold potential of the established pharmaceutic TMZ far beyond the treatment of brain tumors cells and results in an attractive reformulated drug with enhanced therapeutic in-dex

Key words: BioShuttle, Carrier Molecules; Drug Delivery; facilitated Transport; Glioblastoma multiforme (GBM); Reformula-tion, Temozolomide (TMZ)

Introduction

The medicinal treasures in the pharmacopoeia

worldwide, harboring multi-faced monographs,

whose pharmacologic potential albeit their therapeutic

limits are well known New formulations of

conven-tional cytotoxic drugs may open a door to a new

qual-ity of the pharmaceutical research This redesign of

“old fashioned” molecules to highly active

pharma-ceutical ingredients (API) could be a suitable practice

capable of improve the therapeutic index [1-4] In case

of malignant brain tumors especially in the

chemo-therapy of glioblastoma multiforme (GBM) the anti

cancer drug temozolomide (TMZ)

(8-carbamoyl-3-methylimidazo [5,1-d]-1,2,3,5-tetrazin-

4(3H)-one) has been well studied [5, 6] It has been

shown in recent phase III study, that a simultaneous

therapy with TMZ improves survival rates for patients

with GBM treated with radiotherapy [7] Encouraging data [8] give reason to expand the intervention with TMZ to difficult tumor types like prostate cancer Un-der clinical conditions TMZ was absorbed rapidly into the blood, and spontaneously decomposed at physio-logical pH to the cytotoxic methylating agent 5-(3-methyltriazeno)-imidazole-4-carboxamide

(MTIC) Its half-life and apparent oral systemic clear-ance values were 1.8 hours and 97 ml/minute/m2, however neutropenia and thrombocytopenia limited the tolerable application doses to 1000 mg/m2 The cytotoxicity of TMZ appears to be elicited through adduction of methyl groups to O6 positions of guanine (O6mG) in genomic DNA [9] followed by recognition

of this adduct by the mismatch repair system (MMR), which can mispair with thymine during the next cycle

of DNA replication [10, 11]

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The half-life of TMZ [12] in plasma and the

non-target-gene-specific alkylating mode of action can

lead to undesired adverse reactions, which could result

in discontinuation or interruption of therapy TMZ

therefore seems to be a good candidate for

reformula-tion, since our new TMZ derivatives could circumvent

these problems by retaining the high efficiency but not

the adverse effects of TMZ

The coupling of a peptide-based nuclear

localiza-tion sequence (NLS) leads to an active nuclear

target-ing minimiztarget-ing the above described handicaps (Drug

Design, Development and Therapy, in press) But due

to their higher molecular mass and their

phys-ico-chemical characteristics the transport of TMZ-NLS

peptide conjugates alone across the cellular membrane

is poor Therefore a transport molecule is needed so

that a sufficient concentration of pharmacologically

active molecules can reach their target side inside the

nucleus

Our efforts resulted in suitable ligation modes of

TMZ with a nuclear address peptide which in turn is

connected to carrier molecules For a better

under-standing a definition for “ligation” is given in

chemis-try the meaning of “ligation reaction” is the basis of the

Diels-Alder chemistry, which we focus on here

Such a ligation reaction should meet the

follow-ing criteria: (1) rapid course of the reaction, (2)

inde-pendent from solvent properties, (3) no side reaction

with other functional groups present in the molecules,

(4) without additional coupling-reagents, (5)

irreversi-ble chemical reaction characteristics, and (6) an

eco-nomical procedure

Our concept is based on the ‘Click Chemistry’ It’s

applications are increasingly found in all aspects of

drug discovery, ranging from clue finding through

combinatorial chemistry and target-templated in situ

chemistry, to proteomics and DNA research, using

Staudinger and Sharpless conjugation reactions

[13-16] In this regard the 1,3-dipolar cycloaddition

developed by Huisgen has to be considered as a 'cream

of the crop' [17]

Our ligation approach is based on cycloaddition

reactions via the pericyclic Diels Alder Reaction (DAR)

with ‘inverse-electron-demand’ (DARinv), which is a

modification of π-electron-deficient N-heteroaromatics

with electron-rich dienophils [18] The DARinv is, in

contrast to DAR, irreversible with the compounds we

used In this way the pharmaceutic TMZ was coupled

to the modularly structured carrier We called it

TMZ-BioShuttle During biological tests we reached a

dramatically increased efficiency in two different

tu-mor cell lines in the glioblastoma cell line TP 366 and

in the human prostate cancer cell line DU 145

The analyses of dilution series indicated for the application of the TMZ-BioShuttle that the spectra of the treatable tumor types could be extended

Materials and Methods

Synthesis of the TMZ-derivative

A 0.2 mol preparation with 42.7 mg 4-methyl-5-oxo-2,3,4,6,8-pentazabicyclo[4.3.0]nona-2,7,

9-trien-9-carboxylic acid chloride and 67.4 mg

modi-fied tetrazine as well as 28 µl triethylamine were dis-solved in chloroform The reaction process runs un-disturbed and provides a defined product with the molecular weight (MW) m/e 513

Synthesis of the Boc-Lys(TCT)-OH

42 mg cyclooctotetraen and 44 mg maleic acid anhydride were resolved in chloroform and methanol

1 % The chemical reaction is described by Reppe [19]

Solid phase peptide synthesis of the BioShuttle transporter

For solid phase synthesis of the K(TCT)-NLS-S∩S-transmembrane transport peptide the Fmoc-strategy was employed in a fully automated multiple synthesizer (Syro II) [20] The synthesis was carried out on a 0.05mmol Fmoc-Lys(Boc)-polystyrene resin 1% crosslinked and on a 0.053 mmol Fmoc-Cys(Trt)-polystyrene resin (1% crosslinked) As coupling agent 2-(1H-Benzotriazole-1-yl)-1,1,3,3- tetramethyluronium hexafluorophosphate (HBTU) was used The last amino acid of the NLS-peptide was incorporated as Boc-Lys(TCT)-OH Cleavage and de-protection of the peptide resin were affected by treat-ment with 90% trifluoroacetic acid, 5% ethanedithiol, 2.5% thioanisole, 2.5% phenol (v/v/v/v) for 2.5 h at room temperature The products were precipitated in ether The crude material was purified by preparative HPLC on an Kromasil 300-5C18 reverse phase column (20 × 150 mm) using an eluent of 0.1% trifluoroacetic acid in water (A) and 60% acetonitrile in water (B) The peptides were eluted with a successive linear gradient

of 25% B to 60% B in 40 min at a flow rate of 20 ml/min The fractions corresponding to the purified protein were lyophilized

Coupling of the transmembrane carrier - and the K(TCT)-NLS-Cys-module

The K(TCT)-NLS-C and the transport peptide were oxidized in an aqueous solution of 2mg/ml in 20% DMSO After five hours the reaction was com-plete The oxidation progress was monitored by ana-lytical C18 reversed-phase HPLC, and then the peptide was purified as described above The purified material

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was characterized with analytical HPLC and laser

de-sorption mass spectrometry in a Bruker Reflex II

Reagents and cell culture

Human glioblastoma (GBM) primary cells (TP

366) [21] and human prostate cancer cells (DU 145) [22]

were provided by the DKFZ division of Biophysics of

Macromolecules All cell lines were cultured in DMEM

(Gibco Cat No 12800) supplemented with 10% FCS

and maintained in culture at 37°C with 5% CO2

at-mosphere and 95% humidity

Chemotherapy treatment

Pure temozolomide (TMZ) was purchased from

Sigma-Aldrich, Germany (Cat No 76899) and the

material was subdivided into two parts for subsequent

processing One part was followed up and coupled to

the transporter molecules As a control, the second part

was dissolved in acetonitrile 10% (Sigma-Aldrich,

Germany) with a final concentration of 0.2%

acetoni-trile

DU 145 and TP 366 cells were seeded (1 × 105

cells/ml) in DMEM (control) and in DMEM containing

a dilution series of TMZ and of TMZ-BioShuttle from

50 to 6.25 µM respectively The behavior of the cells

was up to 6 days

Cell Cycle Analysis

The effects on the cell cycle distribution were

de-termined by DNA flow cytometry Flow cytometric

analyses were performed using a PAS II flow

cytome-ter (Partec, Muenscytome-ter, Germany) equipped with a

mercury vapor lamp (100 W) and a filter combination

for 2,4-diamidino-2-phenylindole (DAPI) stained

sin-gle cells From native probes the cells were isolated

with 2.1% citric acid/ 0.5% Tween 20 according to the

method for high resolution DNA and cell cycle

analy-ses [23] at room temperature Phosphate buffer (7.2g

Na2HPO4 × 2H2O in 100ml H2O dest.) pH 8.0

contain-ing DAPI for staincontain-ing the cell suspension was

per-formed Each histogram represents 30.000 cells for

measuring DNA-index and cell cycle For histogram

analysis, we used the Multicycle program (Phoenix

Flow Systems, San Diego, CA)

Cell viability

For detection of apoptotic cells and viability, a

FACS Calibur flow cytometer (Becton Dickinson

Cy-tometry Systems, San Jose, CA) was used with filter

combinations for propidium iodide For analyses and

calculations, the Cellquest program (Becton Dickinson

Cytometry Systems, San Jose, CA) was carried out

Each histogram and dot plot represents 10.000 cells

After preparation according to Nicoletti [24] with

modifications [25, 26], measurements were acquired in the logarithmic mode in Fl-3 and calculated by setting gates over the first three decades to detect apoptotic cells Dead cells are positive for propidium iodide and stained red, living cells remain unstained In the loga-rithmic histogram the positions of unstained living cells in a are in the first 2 decades the 3th decade con-tains cells with membrane damage, dead cells are placed in the 4th decade

Results

Time-Course of Cell Growth and comet formation

in DU 145 prostate cancer and TP 366 glioblastoma cells provoked by TMZ and TMZ-BioShuttle dilu-tion series

Two different cell lines originating from different tumor entities like the metastatic human prostate epi-thelium adenocarcinoma, herein referred as DU 145 (Figures 1-2) and TP 366 cells derived from human glioblastoma (Figures 3-4) were used to investigate the pharmacological effect of TMZ and TMZ-BioShuttle

To learn more about the DNA damage and cell death in the two different cell lines after treatment with TMZ as well as with TMZ-BioShuttle using the identical dilution series, we carried out comet assays in parallel probes (right columns of the figure 1 and 2) Basically the untreated cultures of DU 145 prostate cancer cells and TP 366 cells did not exhibit frag-mented DNA

DU 145 Prostate cancer cells

In order to determine the sensitivity of these cells

we used a dilution series in a range from 50 to 6.25 µM

of TMZ and TMZ-BioShuttle respectively

Two days after treatment with the TMZ final concentrations 6.25, 12.5 and 25 µM, the DU 145 cells seemed to be unfazed and no visual change in the phenotype could be observed under the light micro-scope Counting the corresponding cell numbers of-fered a hardly detectable decrease of the cell number (from 1.15 to 1.05 × 106 cells) if anything compared to the untreated control with 1.12 × 106 cells Only the probe treated with 25 µM TMZ revealed a decrease to 0.844 × 106 cells (Figure 1) The comet assay study in-dicated a higher sensitivity and exhibits fragmented DNA in the probes which were treated with 12.5, 25 and 50 µM TMZ The samples treated with 50 µM TMZ displayed a decrease of the cell number to 0.628 × 106 Additionally in the cell culture medium an increasing number of dead, clumped DU 145 cells could be ob-served

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Figure 1 Microscopical monitoring of the human prostate

cancer DU 145 cells 2 days after treatment with TMZ In the

comet column the scale bar represents 20 µm The microscopic

pictures were taken in phase-contrast, enlargement 200×

TP 366 glioblastoma cells

Light microscopical studies showed a reduced

cell population after treatment with 6.25 µM TMZ for 6

days which was increased further diminished under

two fold application doses (12.5; 25 µM) from 6.2 × 105

cells (untreated control) to 5.3; 4.8, and 2.1 × 105 cells In

the TP 366 cells the TMZ probe treated with 50 µM,

however, the cell population remained at the level of

the 25 µM treated cells (2.1 × 105 cells) and may reach a

saturation level

After 6 days treatment with 6.25 µM TMZ (figure

1 and 2) the TP 366 cells showed differently sized and

fragmented dead cells, sporadic comet structures and

shrunken nuclei In relation to the increased

applica-tion doses an increase of fracapplica-tionated DNA and shrunk

nuclei could be observed The TP 366 probe treated

with 50 µM TMZ exhibited sporadic comets and

al-most condensed nuclei The probes treated with

TMZ-BioShuttle displayed a deviant behavior The

6.25 µM TMZ-BioShuttle treated cells offer no DNA

fragmentation, but their nuclei seemed to be partly

swollen and diminished (figure 2) The latter fraction was increasing in accordance to the increased applica-tion doses In addiapplica-tion the total cell count of the TMZ treated samples was lower, compared to the cell number in the control and cells treated with TMZ-BioShuttle

The comet assay study detected no DNA frag-mentation in the untreated control TP 366 cells until

144 hours After application of TMZ-BioShuttle (6.25 µM) and more, much more DNA-fragments could be observed (figure 4) Indeed the use of higher applica-tion doses enhanced DNA fragmentaapplica-tions and the ra-tios of shrunk nuclei of TP 366 (figure 4 right column)

Figure 2 Microscopical monitoring of the human prostate cancer DU 145 cells 2 days after treatment with TMZ-BioShuttle In the comet column, the scale bars in the maps represent 20 µm The microscopic pictures were taken in phase-contrast, enlargement 200×

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Figure 3 Microscopic and comet assay studies of untreated

TP 366 cells and treated with various concentrations of TMZ;

the scale bar represents 20µm

Cell Cycle Studies

Here we present measurements of the cell

activi-ties like the cell cycle analysis using the flow

cytomet-ric method and a calculation of the percentage of cells

in different phases of the cell cycle These data were

obtained after treatment with TMZ and the

TMZ-BioShuttle in depency on the application dose

We determined the cell cycle behaviour of TP 366

glioma cells and DU 145 prostate cancer cells To

in-vestigate the influence of TMZ with and without

BioShuttle transporter we performed a dose-response

analysis of the cell cycle shown in Figures 5 and 6

TP 366 glioblastoma cells treated by TMZ and

TMZ-BioShuttle dilution series

Figure 5 exhibits the cell cycle distribution of TP

366 cells 6 days after treatment with increasing

con-centrations of TMZ and TMZ-BioShuttle is shown in

figure 5 The cell cycle distribution is signed as G1

phase, S phase and the G2/M phase These cells show

a diploid cycle (red coloured) The plot of the

un-treated control is demonstrated (figure 2, line 1) and

exhibits a G1 cell fraction of 86.4 % and a G2 cell

frac-tion 5.7 % Looking the TMZ treated cells the

contin-gent of cells in the S phase amounts to 7.8 % In com-parison to the S phase fraction of untreated control the percentage of S phase cells treated with 6.25 µM TMZ

is increased to 11.1 % The doubling of the TMZ dose to 12.5 µM results in a slightly decrease of the S phase fraction to 9.4 % The further increase of the TMZ concentration to 25 µM and 50 µM has barely influ-enced the amount of the cells in the S phase with 9.1 % and 9.8 % respectively Regarding the G2 phase we observed a dose dependent linear increase of the cell ratio A concentration of 6.25 µM depicted an increase

of cells from 5.7 % (control) to 10.2 % The TMZ dose of 12.5 µM results in a scarcely increase to 10.7 %, but the doubling of the TMZ concentration to 25 µM and fur-ther to 50 µM resulted in an intense increase of the cell fraction in the G2/M phase with 15.9 % and 21.3 % respectively The analysis of the dose dependent effect

on the G1 phase exhibited the following trend: the starting dose rate was 6.25 µM TMZ, doubling of the doses to 25 and to 50 µM showed a reciprocal propor-tionality to the percentage of G1 cells, 74.8% and 68.8% (figure 2, right column)

Figure 4 Microscopic and comet assay of untreated TP 366 glioblastoma cells, and 6 days after treatment with TMZ-BioShuttle; the scale bar represents 20µm Microscopic magnification is 200-fold in the phase contrast microscope

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The TMZ-BioShuttle treated TP 366 cells

pre-sented a cell cycle behaviour strongly differing from

the untreated control and from the TMZ treated cells

The probe treated with 6.25 µM evidenced a

re-duced cell fraction in G1 phase of 70.6% already The

TP366 cells treated with doses 12.5 and 25 µM indicate

G1 ratios of 57.9 and 37.6% respectively Especially the

data of the G2/M phase are demonstrative From 6.25

µM up to 25 µM we observed an increase of the ratio of

cells in G2/M from 19.1 %, via 28.6 % to 37.6 % In

comparison with the corresponding TMZ data, we

found a continuous G2/M enhancement with the

fac-tor 2 starting at 6.25 µM! to 25 µM and a facfac-tor 3 in the

probes treated with 12.5 µM

Due to the high amount of

dead cells the estimation of the

cell cycle distribution in TP 366 cells treated with 50

µM TMZ-BioShuttle was difficult to perform and to analyse It shows an increase of the cell fraction in the G1 phase to 68.8% which is identical to the corre-sponding probe treated with TMZ Consistently in-creased amounts of the S phase cells could be detected compared to both the S phase in the control and the corresponding probes treated with TMZ The trend of G2/M phase cells turned to the opposite direction In the S phase not definitive trend arose from the applied dose

Figure 5 The cell cycle distribution

in TP 366 glioblastoma cells dependent

on the applied concentration of TMZ

(right column) and TMZ-BioShuttle

(left column) 6 days after treatment

The axes of coordinates represent the

cell number; the abscissae represent the

corresponding DNA content The left

peak depicts the amount of cells in the

G1 phase; the area of the right peak

describes the ratio of cells in the G2/M

phase The area between both peaks

displays the amount of the cell fraction

residing in the S phase The insert

de-scribes the percentage of cells in the

phases of the cell cycle

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Figure 6 The cell cycle ratio of DU 145 prostate cancer cells dependent on the applied concentration of TMZ (right column) and TMZ-BioShuttle (left column) 2 days after treatment The axes of coordinates represent the cell number; the abscissae represent the corresponding DNA content The left peak depicts the amount of cells in the G1 phase; the area of the right peak describes the ratio

of cells in the G2/M phase The area between both peaks displays the amount of the cell fraction residing in the S phase

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Cell cycle behaviour of DU 145 cells after treatment

with TMZ and TMZ-BioShuttle dilution series

At a first glance the histograms reveal a lower

sensitivity of DU 145 prostate cells against TMZ

treatment compared to the results of TP 366 cells The

untreated DU 145 control exhibits a cell cycle

distribu-tion as follows: G1 – 58.5%; S phase – 29.8% and G2/M

phase 11.6% The ratio of TMZ treated cells in the

G2/M phase amounts to 12.8%; 15.4% and 23.5% and

is constantly increasing in correlation to the

applica-tion doses of 6.25; 12.5 and 25 µM

The percentage of the S phase cells after treatment

with the above described concentrations were almost

constant 29.5% and close to the control The cells in the

G1 fractions treated with increasing concentrations up

to 25 µM of TMZ presented a moderate but uniform,

continuous decrease from 58.5% (control), via 57.5%,

56.4%, to 48.6 % and then a strong decline to 29.8%

The DU 145 probe treated with 50 µM TMZ showed

22.3% G2/M phase cells and a dramatic increase of the

S phase cell fraction to 47.7%

The DU 145 cells treated with the TMZ-BioShuttle

under identical conditions offered a cell cycle

behav-iour which strongly differs from the TMZ probes The

percentage of cell fractions in G1 phase seemed to be

nearly constant 58.5% comparing the untreated control

versus the treated cells with concentrations 6.25µM

59.2 %and 12.5 µM 57.4% The concentrations of 25 and

50 µM gave rise to a marked decrease of the percentage

of cells from 45.5% to 20.7% in G1 which corresponds

to one-third of the related TMZ treated probe!

The relative amounts of S phase cells in the con-centration series with increasing TMZ-BioShuttle doses of 6.25, 12.5, 25, and 50 µM offered a reciprocal proportionality and showed a small but continuous decrease of cell number from 29.8% (control), via 28.8%, 28.1%, 27.1%, to 24.2% respectively It is im-portant to note that the latter result showed a strong reduction comparing 47.7% (TMZ) to 24.2% (TMZ-BioShuttle) which equates a degression of 50% The concentration series with increasing amounts of TMZ-BioShuttle indicated a direct concentration de-pendence and displayed a moderate increase of the cell number of DU 145 cells in the G2/M fraction from 11.6% (control) to 11.9% in the 6.25 µM probe via 12.5,

25 to 50 µM A strong rise of the S phase cells from 14.6% via 27.4% to 55.1% was shown Doubling the applied dose increased cell number in the G2/M phase mote than 100%! Additionally, the direct comparison

of the probe treated with 50 µM TMZ-BioShuttle with the corresponding TMZ probe of DU 145 cells showed

a dramatic increase in the percentage of cells in the G2/M phase (from 22.3% to 55.1%), revealing a G2/M block

Figure 7 The dose dependent effects of TMZ (C/D) as well as TMZ-BioShuttle (A/B) in the cell cycle behaviour of TP366 glioma (A/C) and DU 145 prostate cancer (B/D) cells ♦ G1phase; „ S phase; S G2/M phase

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Discussion

The number of old-fashioned cytotoxic drugs,

whose effectiveness is well understood, is multi-faced

However, if highly effective substances do not reach

their target site after application, what is their benefit?

Therefore questions about the bioavailability remain to

be answered, whereby the concentration in the

blood-stream is not meant here, but rather the concentration

directly at the site of pharmacological action, like the

genomic DNA in tumor cell nuclei

A substantial progress in the drug development

will be achieved by improvement of the delivery and

subcellular targeting of the drug as yet unappreciated

and meaningless

The BioShuttle delivery and targeting platform,

facilitating the transport of DNA derivatives into

liv-ing cells was described [27, 28] as well as transport of

diagnostics into the cytoplasm and nuclei of tumor

tissues [29, 30] There is no doubt that constructs like

the TMZ-BioShuttle, as an example, could play a

helpful role in the treatment of cancer The design of

such shuttles needs to incorporate features that reduce

undesired adverse reactions but maintains the efficacy

We selected the highly efficient chemotherapeutic

TMZ as a qualified candidate, since encouraging

re-sults in treatment of in brain tumors [31] remain

un-endorsed in the treatment of hormone-refractory

prostate cancer (HRPC) [32]

Parallel sets of experiments with TP 366 glioma

cells and DU 145 prostate cancer cells were carried out

and confirmed a lesser sensitivity of DU 145 prostate

cancer cells against TMZ treatment Whereas the TP

366 cells showed an increased DNA damage after TMZ

treatment up to a final concentration of 6.25 µM, the

DU 145 cells exhibited very few DNA damage

meas-ured by comet assay The increase of the application

dose however did not induce an increased number of

comets (figure 1) This phenomenon was already

documented in studies with ceramide-induced cell

death [33]

In DU 145 cells we compared the dose-dependent

application of TMZ and TMZ-BioShuttle of seeded

versus harvested cells after 48 hours In comparison to

the control (1.12) a linear inverse proportionality (1.15;

1.05; 0.844; and 0.628) to the dilution series of 6.25; 12.5;

25; and 50 µM TMZ was demonstrated

These data permit to assume a minimum of TMZ

application dose between 25 and 12.5 µM Dilution

series with 50 µM to 6.25 µM of TMZ-BioShuttle

showed an increase of shrunk nuclei (figures 2 and 4)

The TMZ-BioShuttle revealed the identical

subthresh-old in DU 145 cells but the quotient 0.414 at 50 µM suggests a higher pharmacological potential

The results achieved with both cell lines (TP 366 and DU 145) treated with the TMZ-BioShuttle differ in the expected augmentation of DNA comets: All cells were visibly swollen, but we could not detect an in-creased number of comets This suggests a deconden-sation of chromatin in the nuclei This happens when chromosomes are exposed to DNA replication inhibi-tion caused by failure to constitute compact chromatin areas during mitosis [34] It could be explained with the involvement of the transcription of genes express-ing histone regulatexpress-ing proteins responsible for forma-tion of the chromatin structure and for the compact package of DNA [35]

We investigated the cell cycle of TP366 after treatment of the glioblastoma cells with TMZ It inter-fered with the cell cycle and exhibited a decreased number of cells in the S phase fraction as shown 144 hours after TMZ-application when a contingent of the

S phase cells of 8% was detectable

The phenomenon of a reduced S phase (8% ver-sus control 11%) in the TMZ treated TP 366 cells is not contradictory to the common effects of alkylating agents which cause a retardation of the rate of cell di-vision [36] A possible explanation for the strongly decreased S phase cell number in the TMZ-BioShuttle treated probes would be the existence of a S phase cell cycle arrest as documented in a bimodal TMZ/ inter-feron-β (IFN-β) study [37] Our flow cytometry ex-periments also displayed a strong cell cycle arrest in the S phase [38] An interesting criterion for a pro-longed late S/G2 phase suggests the implication of the histone acetyltransferase 1 (HAT1) which participates

in recovering block-mediated DNA damages [39] The fact that the glioblastoma cells arrest in the G2/M phase after TMZ-treatment was documented by Hirose et al [40] and could be confirmed with the TP

366 cells Moreover the treatment with TMZ-BioShuttle resulted in a clearly increased G2/M phase of 72% It seems to be attributed to interactions of TMZ and TMZ-BioShuttle with the mitogen-activated protein (MAP) kinase p38α, which is activated by the mis-match repair system (MMR) and is responsible for the TMZ-induced G2/M block [40]

After cell exposure to the TMZ-BioShuttle for 144 hours, the observed strong increase of the G2 phase cells of TP 366 cells possibly originate from the already documented inhibition of the RNA and protein syn-theses, which are necessary for the successful comple-tion of G2 and the initiacomple-tion of mitosis These G2-arrested cells were found to be deficient in certain proteins that may be specific for the G2-mitotic

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transi-tion [41] The obstructransi-tion of the cell cycle process is

caused by the stop of this transition and results in the

decrease of the G1 phase cell fraction (26%) of the

TMZ-BioShuttle treated TP 366 cells which appear to

be consequence of their disability passing in the

mi-totic process

A sensitivity of DU 145 and TP 366 cells against

TMZ and a dramatically increased sensibility against

TMZ-BioShuttle is shown in figure 4 The present data

document a different cellular contumaciousness to

TMZ treatment A real effectiveness of the pure TMZ

in DU 145 cells could not be observed, whereas in

contrast clear cell killing effects, caused by

TMZ-BioShuttle, were detected

It is important to note that the TMZ-BioShuttle

treatment of DU 145 and the TP 366 cells redounds to

cell killing effects as shown in figure 4

As a general rule the different sensitivity of tumor

cells against chemotherapeutics is dependent on

mul-tiple mechanisms like mulmul-tiple drug resistance

sys-tems The relative low sensitivity of DU 145 prostate

cancer cells after treatment with TMZ is evident, and

the disappointing results of TMZ trials of prostate

cancer can be explained by the increased

O6-methylguanine-DNA methyltransferase (MGMT)

repair activity DU 145 cells show an increased MGMT

activity [42], associated with the decrease of the

pharmacologic effect after alkylating with TMZ alone

The increased MGMT expression and activity

corre-lates with the malignant phenotype [43] We regard the

potential utility of this epigenetic alteration as an

ap-propriate biomarker for prostate cancer [44] and an

important prognostic feature for the clinical outcome

in glioblastoma [45] The fact that die blood brain

bar-rier (BBB) no presents an hurdle for TMZ could explain

the higher pharmacological effects of TMZ in glioma

cells It is important in so far that the delivery and the

targeting of active substances play a decisive role and

must be further scrutinized The TMZ-BioShuttle could

be an appropriate candidate

The physico-chemical properties of TMZ which

have an impact on its bioavailability limit its

pharma-cological effectiveness Despite the benefit of the

con-comitant treatment with radiotherapy plus TMZ,

he-matologic toxic effects in patients treated with TMZ

are documented in multicenter studies by Stupp [46]

A TMZ-derivatization with targeting transporters

molecules and subcellular address components holds

tremendous potential to optimize treatment of

dis-eases Enhanced cellular delivery and active transport

of TMZ into the cell nuclei as site of pharmacological

action permit to expect lower application doses with

concomitantly decreased limiting side-effects

Our shuttle, designed for facilitating the rapid transport across cellular membranes, improved their own delivery and their own targeting under per-petuation of the pharmacological activity in cells and tissues while protecting cells in the bloodstream by omission of undesired side-effects like:

Strong suppression of the peripheral lympho-cytes result in discontinuation of therapy and prob-lems associated with systemic drug administrations, which are:

• even biodistribution of pharmaceuticals through-out the body;

• the lack of drug specific affinity toward a patho-logical site;

• the necessity of a large total dose of a drug to achieve high local concentration;

• non-specific toxicity and strong adverse side-effects due to high drug doses [47, 48]

The application of the TMZ-BioShuttle could minimize the handicap of TMZ on the therapy of pa-tients with brain tumors but the establishment of the TMZ-BioShuttle necessitates new ways for the synthe-sis Conditions which hampered the above postulated criteria like rapid and whole concurrent chemical re-actions in aqueous solution at room temperature for a proper chemical ligation of functional peptides could

be circumvented using the ‘inverse-electron-demand’

of the Diels Alder Reaction

Thus, TMZ-BioShuttle has been reformulated to decrease the toxic features in normal cells but retain the pharmacologic behavior in target cells; this was achieved as follows: coupling the amide group of the TMZ with a tetrazine which acts as dien-component and connects the NLS module with the tridecadien (TCT) component operating as dienophil

The presented publication shows that a proper chemistry contributes to the optimization of the pharmacological properties of the already efficient pharmaceutics like TMZ

The novel properties of the TMZ-BioShuttle could give reason to the extension to tumor types like pros-tate cancer, especially in hormone refractory situa-tions

Abbreviations

DAR: Diels-Alder-Reaction, GBM: Glioblas-toma Multiforme, HAT1: Histone Acetyltransferase 1, IFN-β: Interferon-β, MGMT: Methylgua-nine-DNA-Methyltransferase, NLS: Nuclear Localiza-tion Sequence, TCT: Tetracyclo-[5.4.21,7.O2,6.O8,11] 3,5-dioxo-4-aza-9,12-tridecadien, TMZ: Temozo-lomide

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